Ventricular fibrillation pathophysiology: Difference between revisions
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Familial conditions that predispose individuals to developing ventricular fibrillation and [[sudden cardiac death]] are often the result of [[gene mutation]]s that affect cellular transmembrane ion channels. For example, in [[Brugada syndrome]], sodium channels are affected. In certain forms of [[long QT syndrome]], the potassium inward rectifier channel is affected. | Familial conditions that predispose individuals to developing ventricular fibrillation and [[sudden cardiac death]] are often the result of [[gene mutation]]s that affect cellular transmembrane ion channels. For example, in [[Brugada syndrome]], sodium channels are affected. In certain forms of [[long QT syndrome]], the potassium inward rectifier channel is affected. | ||
===Triggered Activity=== | ===Triggered Activity=== | ||
Triggered activity can occur due to the presence of | Triggered activity can occur due to the presence of afterdepolarisations. These are depolarising oscillations in the membrane voltage induced by preceding [[action potential]]s. These can occur before or after full repolarisation of the fiber and as such are termed either early (EADs) or delayed afterdepolarisations (DADs). All afterdepolarisations may not reach threshold potential, but if they do, they can trigger another afterdepolarisation, and thus self-perpetuate. | ||
===Abnormal Automaticity=== | ===Abnormal Automaticity=== | ||
Automaticity is a measure of the propensity of a fiber to initiate an impulse spontaneously. The product of a [[Hypoxia (medical)|hypoxic]] myocardium can be hyperirritable myocardial cells. These may then act as pacemakers. The ventricles are then being stimulated by more than one [[pacemaker]]. Scar and dying tissue is inexcitable, but around these areas usually lies a penumbra of hypoxic tissue that is excitable. Ventricular excitability may generate re-entry arrhythmias. | Automaticity is a measure of the propensity of a fiber to initiate an impulse spontaneously. The product of a [[Hypoxia (medical)|hypoxic]] myocardium can be hyperirritable myocardial cells. These may then act as pacemakers. The ventricles are then being stimulated by more than one [[pacemaker]]. Scar and dying tissue is inexcitable, but around these areas usually lies a penumbra of hypoxic tissue that is excitable. Ventricular excitability may generate re-entry arrhythmias. | ||
Revision as of 15:16, 17 January 2013
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Ventricular fibrillation Microchapters |
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Differentiating Ventricular Fibrillation from other Diseases |
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Risk calculators and risk factors for Ventricular fibrillation pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Ventricular fibrillation is a cause of cardiac arrest and sudden cardiac death. The ventricular muscle twitches randomly rather than contracting in a coordinated fashion (from the apex of the heart to the outflow of the ventricles), and so the ventricles fail to pump blood into the arteries and systemic circulation. Ventricular fibrillation is a sudden lethal arrhythmia responsible for many deaths in the Western world, and it is mostly caused by ischemic heart disease. While most episodes occur in diseased hearts, others can afflict normal hearts as well. Despite considerable research, the underlying nature of ventricular fibrillation is still not completely understood.
Pathophysiology
Ventricular fibrillation has been described as "chaotic asynchronous fractionated activity of the heart" (Moe et al. 1964). A more complete definition is that ventricular fibrillation is a "turbulent, disorganized electrical activity of the heart in such a way that the recorded electrocardiographic deflections continuously change in shape, magnitude and direction".[1]
Ventricular fibrillation most commonly occurs within diseased hearts, and, in the vast majority of cases, is a manifestation of underlying ischemic heart disease. Ventricular fibrillation is also seen in those with cardiomyopathy, myocarditis, and other heart pathologies. In addition, it is seen with electrolyte disturbances and overdoses of cardiotoxic drugs. It is also notable that ventricular fibrillation occurs where there is no discernible heart pathology or other evident cause, the so-called idiopathic ventricular fibrillation.
Idiopathic ventricular fibrillation occurs with a reputed incidence of approximately 1% of all cases of out-of-hospital arrest, as well as 3%-9% of the cases of ventricular fibrillation unrelated to myocardial infarction, and 14% of all ventricular fibrillation resuscitations in patients under the age of 40.[2] It follows then that, on the basis of the fact that ventricular fibrillation itself is common, idiopathic ventricular fibrillation accounts for an appreciable mortality. Recently-described syndromes such as the Brugada syndrome may give clues to the underlying mechanism of ventricular arrhythmias. In the Brugada syndrome, changes may be found in the resting ECG with evidence of right bundle branch block (RBBB) and ST elevation in the chest leads V1-V3, with an underlying propensity to sudden cardiac death.[3]
The relevance of this is that theories of the underlying pathophysiology and electrophysiology must account for the occurrence of fibrillation in the apparent "healthy" heart. It is evident that there are mechanisms at work that we do not fully appreciate and understand. Investigators are exploring new techniques of detecting and understanding the underlying mechanisms of sudden cardiac death in these patients without pathological evidence of underlying heart disease.[4]
Familial conditions that predispose individuals to developing ventricular fibrillation and sudden cardiac death are often the result of gene mutations that affect cellular transmembrane ion channels. For example, in Brugada syndrome, sodium channels are affected. In certain forms of long QT syndrome, the potassium inward rectifier channel is affected.
Triggered Activity
Triggered activity can occur due to the presence of afterdepolarisations. These are depolarising oscillations in the membrane voltage induced by preceding action potentials. These can occur before or after full repolarisation of the fiber and as such are termed either early (EADs) or delayed afterdepolarisations (DADs). All afterdepolarisations may not reach threshold potential, but if they do, they can trigger another afterdepolarisation, and thus self-perpetuate.
Abnormal Automaticity
Automaticity is a measure of the propensity of a fiber to initiate an impulse spontaneously. The product of a hypoxic myocardium can be hyperirritable myocardial cells. These may then act as pacemakers. The ventricles are then being stimulated by more than one pacemaker. Scar and dying tissue is inexcitable, but around these areas usually lies a penumbra of hypoxic tissue that is excitable. Ventricular excitability may generate re-entry arrhythmias.
It is interesting to note that most cardiac myocardial cells with an associated increased propensity to arrhythmia development have an associated loss of membrane potential. That is, the maximum diastolic potential is less negative and therefore exists closer to the threshold potential. Cellular depolarisation can be due to a raised external concentration of potassium ions K+, a decreased intracellular concentration of sodium ions Na+, increased permeability to Na+, or a decreased permeability to K+. The ionic basic automaticity is the net gain of an intracellular positive charge during diastole in the presence of a voltage-dependent channel activated by potentials negative to –50 to –60 mV.
Myocardial cells are exposed to different environments. Normal cells may be exposed to hyperkalaemia; abnormal cells may be perfused by normal environment. For example, with a healed myocardial infarction, abnormal cells can be exposed to an abnormal environment such as with a myocardial infarction with myocardial ischaemia. In conditions such as myocardial ischaemia, possible mechanism of arrhythmia generation include the resulting decreased internal K+ concentration, the increased external K+ concentration, norepinephrine release and acidosis.[5] When myocardial cell are exposed to hyperkaliemia, the maximum diastolic potential is depolarized as a result of the alteration of Ik1 potassium current, whose intensity and direction is strictly dependant on intracellular and extracellular potassium concentrations. With Ik1 suppressed, an hyperpolarizing effect is lost and therefore there can be activation of funny current even in myocardial cells (which is normally suppressed by the hyperpolarizing effect of coexisting potassium currents). This can lead to the instauration of automaticity in ischemic tissue.
Re-entry
The role of re-entry or circus motion was demonstrated separately by Mines and Garrey.[6] Mines created a ring of excitable tissue by cutting the atria out of the ray fish. Garrey cut out a similar ring from the turtle ventricle. They were both able to show that, if a ring of excitable tissue was stimulated at a single point, the subsequent waves of depolarisation would pass around the ring. The waves eventually meet and cancel each other out, but, if an area of transient block occurred with a refractory period that blocked one wavefront and subsequently allowed the other to proceed retrogradely over the other path, then a self-sustaining circus movement phenomenon would result. For this to happen, however, it is necessary that there be some form of non-uniformity. In practice, this may be an area of ischaemic or infarcted myocardium, or underlying scar tissue.
It is possible to think of the advancing wave of depolarisation as a dipole with a head and a tail. The length of the refractory period and the time taken for the dipole to travel a certain distance—the propagation velocity—will determine whether such a circumstance will arise for re-entry to occur. Factors that promote re-entry would include a slow-propagation velocity, a short refractory period with a sufficient size of ring of conduction tissue. These would enable a dipole to reach an area that had been refractory and is now able to be depolarised with continuation of the wavefront.
In clinical practice, therefore, factors that would lead to the right conditions to favour such re-entry mechanisms include increased heart size through hypertrophy or dilatation, drugs which alter the length of the refractory period and areas of cardiac disease. Therefore, the substrate of ventricular fibrillation is transient or permanent conduction block. Block due either to areas of damaged or refractory tissue leads to areas of myocardium for initiation and perpetuation of fibrillation through the phenomenon of re-entry.
Characteristics of the ventricular fibrillation waveform
Ventricular fibrillation can be described in terms of its electrocardiographic waveform appearance. All waveforms can be described in terms of certain features, such as amplitude and frequency. Researchers have looked at the frequency of the ventricular fibrillation waveform to see if it helps to elucidate the underlying mechanism of the arrhythmia or holds any clinically useful information. More recently, Gray has suggested an underlying mechanism for the frequency of the waveform that has puzzled investigators as possibly being a manifestation of the Doppler effect of rotors of fibrillation.[7] Analysis of the fibrillation waveform is performed using a mathematical technique known as Fourier analysis.
Power spectrum
The distribution of frequency and power of a waveform can be expressed as a power spectrum in which the contribution of different waveform frequencies to the waveform under analysis is measured. This can be expressed as either the dominant or peak frequency, i.e., the frequency with the greatest power or the median frequency, which divides the spectrum in two halves.
Frequency analysis has many other uses in medicine and in cardiology, including analysis of heart rate variability and assessment of cardiac function, as well as in imaging and acoustics.[8][9]
References
- ↑ Robles de Medina EO, Bernard R, Coumel P; et al. (1978). "Definition of terms related to cardiac rhythm. WHO/ISFC Task Force". Eur J Cardiol. 8 (2): 127–44. PMID 699945.
- ↑ Viskin S, Belhassen B (1990). "Idiopathic ventricular fibrillation". Am. Heart J. 120 (3): 661–71. doi:10.1016/0002-8703(90)90025-S. PMID 2202193.
- ↑ Brugada P, Brugada J (1992). "Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report". J. Am. Coll. Cardiol. 20 (6): 1391–6. doi:10.1016/0735-1097(92)90253-J. PMID 1309182.
- ↑ Saumarez RC, Heald S, Gill J; et al. (1995). "Primary ventricular fibrillation is associated with increased paced right ventricular electrogram fractionation". Circulation. 92 (9): 2565–71. PMID 7586358.
- ↑ Ho K 1993
- ↑ Mines GR 1913, Garrey WE 1914
- ↑ Jalife J, Gray RA, Morley GE, Davidenko JM (1998). "Self-organization and the dynamical nature of ventricular fibrillation". Chaos. 8 (1): 79–93. doi:10.1063/1.166289. PMID 12779712.
- ↑ Shusterman V, Beigel A, Shah SI; et al. (1999). "Changes in autonomic activity and ventricular repolarization". J Electrocardiol. 32. Suppl: 185–92. doi:10.1016/S0022-0736(99)90078-X. PMID 10688324.
- ↑ Kaplan SR, Bashein G, Sheehan FH; et al. (2000). "Three-dimensional echocardiographic assessment of annular shape changes in the normal and regurgitant mitral valve". Am. Heart J. 139 (3): 378–87. doi:10.1016/S0002-8703(00)90077-2. PMID 10689248.